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MEDICAL MICROBIOLOGY

STI (STD)
BY DR NAMKINGA, L.A
May, 2016
STI
• Definition:
– Sexual transmitted infections
– Sexuality = erotic stimulation, genital respons
e to sexual desire
– Formerly venereal disease (VD) or Sexually tr
ansmitted diseases (STD)
– Is an illness that has a significant possibility o
f transmission between humans or animals by
means of sexual contact, including vaginal int
ercourse, oral sex, & anal sex
Top Ten Aetiologic Agents of S
TI
• Neisseria gonorrhea>> gonorrhea
• Treponema pallidum>> syphilis
• Trichomonas vaginalis>> vaginitis, urethriti
s (trichomoniasis)
• Chlamydia trachomatis L1-L3 serotype>> l
ymphogranuloma venerium
• Chlamydia trachomatis>> non-specific uret
hritis
• Papillomaviruses>> genital warts
Top Ten Aetiologic Agents of S
TI 2
• HIV>> AIDS
• Haemophilus ducreyi>> chancroid
• Herpes simplex virus>> genital herpes
• Candida spp**>> vaginal thrush, balanitis
• Hepatitis B virus>> hepatitis (especially m
ale homosexuals)
Part I:
Gonorrhea
• N. gonorrhea:
– Gram negative aerobic diplococcus, in stained
films tend to lie in pairs with their adjacent sid
es flattenedto give a bean-like or kidney shap
ed appearance, this arrangement is best seen
in smears from infected exudates than from c
ultures.
N. gonorrhea Cont…
– They are fastidious, & grow on enriched medi
a e.g. Heated blood agar, or chocolate agar (
Modified Thayer Martin’s agar; selected medi
um for samples with mixed flora) at 37C in 5
% CO2 plus increased humidity. Colonies dev
elop in 48h, non haemolytic, oxidase positive
– Colonies, grey translucent, 1-2mm diam. Four
biotypes distinguished by colonial morphology
. Type 1&2 are fimbriated pathogenic forms. C
apsules on fresh strains
N. Gonorrhea Cont…

• N. gonorrhea ferments glucose but not mal


tose or sucrose
• Sixteen serotypes can be distinguished by
antigenic differences in outer protein mem
brane
Types of Infections
• Depending on one’s sexual inclination:
– Urethral gonorrhea
– Anal-Rectal gonorrhea
– Endo-cervical gonorrhea
– Pharyngeal gonorrhea
– Conjunctival gonorrhea (Ophthalmia neonator
um)
– Oral gonorrhea etc
Pathogenesis of Gonorrhea
• Transmission of infection usually by sexual inter
course, but in the tropics the organism may rem
ain viable on cloth for several hours/days >> vulv
o-vaginitis in children (from beddings, towels, clo
th etc contaminated by moist infective discharge
s)
• Incubation period 2-5 days depending on infectiv
e dose and the type
Pathogenesis of Gonorrhea Cont…

• The risk for men after single intercour


se is 20%. Increases to 60-80% after
4 or more exposures
• In women 90% but no controlled studi
es for number of exposure
• The transmission rate from male>fem
ale is higher than female>male
Pathogenesis of Gonorrhea Cont…
• Columnar epithelium is most susceptible. In mal
e the anterior urethra & urethral glands are the p
rimary sites of infect, from which org can spread
to the posterior urethra, prostate & seminal vesic
les, epididymis & testis & occasionally to the blo
od stream
• In females the cervix is the primary site, spread
to the fallopian tubes, to the peritoneum
Pathogenesis of Gonorrhea Cont…
• Organism attach to & are engulfed by non-ciliate
d cells
• Damage some ciliated cells in the vicinity
• Transit the epithelial layer
• Find access to the basement lamina & sub-muco
sal regions
• Form sub-mucosal abscesses
• Become disseminated in the lymphatic or blood
vascular systems
Clinical manifestations
• Urethral infection in man,Symptoms:
– Dysuria, urethral discharge (purulent), painful micturat
ion due to oedema & erythema of the urethral meatus
(urethritis), and acute epididymitis
– If untreated 95% of pts become asymptomatic in 6 mo
nths. But develop complications:
• Penile lymphangitis, sometimes associated with regional lym
phadenitis
• Penile oedema (bull-headed-clap)
• Chronic prostatitis (posterior urethritis associated with urinary
agency)
• Seminal vesiculitis
Clinical manifestations
• Infection in women:
– Endocervical canal is the primary site
– Urethral colonization is common in hysterecto
mized women
– Incubation period in female is longer ~10 days
(less certainity)
– Symptoms:
• Vaginal, cervical, & batholin discharges. Dysuria, i
nter-menstrual uterine bleeding or menorrhagia. Er
ythema and painful menstruations
Gonorrhea in women 2
• The woman may complain of vaginal discharg
e, difficulty urinating (dysuria), off-cycle mens
trual bleeding, or bleeding after sexual interco
urse. The cervix may appear anywhere from no
rmal to the extreme of marked cervical inflam
mation with pus Increased production of male
hormones is common in many cases. Infection
of the urethra (urethritis) causes little dysuria o
r pus
Clinical manifestations
• Assessment of signs & symptoms in wome
n with gonorrhea is confounded, however,
by co-existing cervico-vaginal infections e.
g. trichomoniasis, chlamydiasis, Gardnerel
la vaginalis vaginitis & Candida vaginitis
Clinical manifestations 2
• If untreated 95% of pts become asyptomatic. But
with complications:
– Pelvic inflammatory disease (PID) here the organis
ms progress to the fallopian tubes causing inflammati
on abscesses>> to severe lower abdominal pain, feve
r & tenesmus & very painful menstruation. Fibrosis &
sterility are the late complications
– The infection may disseminate to the peritoneum. Blo
od borne infect>>bacteremia &meningitis may occur
Pelvic Inflammatory Diseases (P
ID)
• Is a generic term for inflammation of the female
uterus, fallopian tubes, and /or ovaries as it prog
resses to scar formation with adhesions to nearb
y tissues & organs. This may lead to tissue necr
osis with or without abscess formation. Pus can
be released into the peritoneum
• PID is a vague term & can refer to viral, fungal, p
arasitic, though most often bacterial infections (S
TD) is the cause
Salpingitis
• Is an infection & inflammation in the fallopian tub
es
• Often used synonymously with PID, although PI
D lacks an accurate definition & can refer to sev
eral diseases of the female upper genital tract: e
ndometritis, myometritis, parametritis & infect in t
he pelvic peritoneum
• Salpingitis only refer infect & inflammation in the
fallopian tubes
Cont. Salpingitis
• Two types: acute and chronic
• Acute salpingitis: causes the fallopian tubes to b
e red & swollen. The inner walls get adhered to
each other, causing a block in the tube, sometim
es can also get stuck to the surrounding intestin
es
• Chronic salpingitis: is milder, showing lesser sy
mptoms. Often occurs after an attack of acute sa
lpingitis, & lasts longer than acute
Symptoms of Salpingitis
• Pain during ovulation
• Pain during sexual intercourse
• Lower abdominal pain
• Lower back pain
• Pain coming & going in periods
• Abnormal smell and color of vag discharge
• Fever, chills, nausea, vomiting
Bacteria Associated with Salpin
gitis
• Neisseria gonorrhea
• Staphylococcus aureus
• Chlamydia trachomatis
• Mycoplasma
• Streptococcus pyogenes
What Facilitates them to Ascend
?
• Factors which facilitate bacteria to ascend
from the vagina to the fallopian tubes:
– Intra-uterine device (IUD) related
– Uterine contractions/ menstruation
– Sperm, carrying the organisms upwards
– Endometrial biopsy
– Hysteroscopy
– Curettage
Other Clinical manifestations of
Gonorrhea
• Anorectal infections:
– 5% of women and 40% of homosexuals
– Symptoms:
• Anal pruritus, painless muco-purulent discharge &
scant rectal bleeding. To some pts>> overt acute p
roctitis, including severe rectal pain, tenesmus & c
onstipation
• External examination rarely reveals symptoms, but
anoscopy often shows mucoid or purulent exudate
often localized to the anal crypts
Other Clinical manifestations of
Gonorrhea cont…
• Pharyngeal infections & oral infections:
– Results from oral sex >> pharyngitis but some
times asymptomatic

• Ophthalmia neonatorum:
• Intense inflammatory response of the conjunctival
epithelium,giving yellowish exudate of polymorpho
nuclear leukocytes
• Ulceration and thinning of the cornea >> to blindne
ss
Treatment
• Spectinomycin (Togamycin)
• Penicillins (for non NGPP mutants)
• Cephalosporins (second generation)
• Tetracyclins and Erythromycins
Treatment for PID & Salpingitis
• Severe cases: I.V. cefoxitin 2g/ 6hrly for th
e first 24hrs, Followed by doxycycline 100
mg bd + Metronidazole 400mg tds 5days
• Ofloxacin 400mg bd/ 14days + Metronidaz
ole 400mg tds 5d
• Mild cases: Tetracycline 500mg tds 7-10d
+ metronidazole 400mg tds 5/7d
Differential Diagnosis
• Appendicitis
• Ectopic pregnancy
• Septic abortion
• Ruptured ovarian cysts or tumors
• Twisted ovarian cyst
• Degeneration of a myoma
• Acute enteritis
Part II:
Chlamydiae
• Chlamydiasis:
• By Chlamydia trachomatis: Obligate intrac
ellular organisms of 0.25µm diameter. Stai
n with Giemsa or Machiavello’s stain
• Do not grow in bacteriological media, but c
an be cultivated in yolk sac of chick embry
o & in tissue culture
Infections
• Types of infections:
– Lymphogranuloma venereum- caused by ser
otypes L1-L3 of C. trachomatis group A
– Non-gonococcal urethritis, cervicitis, salpingiti
s- caused by serotypes D-K
Signs & symptoms of both above infections ar
e confounded, however, by co-existing cervic
o-vaginal infections e.g. trichomoniasis, gonor
rhea, Gardnerella vaginalis vaginitis & Candid
a vaginitis
Diagnosis & Treatment
• Pt with active infection posses 90-99% IgG
antibodies to the organisms during serolog
ical diagnosis

• Drugs of choice- Tetracyclines


– Others: Erythromycin, Rifampicin and Sulpho
namides
Other Infections by
C trachomatis
• 1) Trachoma- an eye infection caused by
serotypes A, B, C
• Endemic in areas of low rainfall e.g. Dodo
ma, Singida and Arusha
• Transmission by direct contact>> severe e
ye disease, leading to conjunctiva deformit
ies>> 2° infection lead to blindness
Cont. Other Infections by
C trachomatis
• 2) Inclusion conjunctivitis caused by seroty
pes D-K (also agent for non-gonococcal ur
ethritis)
• Infants are infected during birth leading to i
nclusion conjunctivitis (like mild trachoma)
• 3) Respiratory infections- also by serotype
s D-K
• Control: Hygiene
Part III:
Chancroid
• Causative agent: Haemophilus ducreyi
– Gram negative cocco-bacilli
• After entry into the body a papule lesion d
evelops within the epithelium causing swel
ling & white blood cell infiltration. Incubatio
n 4-7 days
• Within several days a pustule forms & rupt
ures
Chancroid cont…
• Is a sexually transmitted disease, caused by H.
ducreyi
• H. ducreyi is a Gram negative, cocco-bacilli
• Chancroid presents itself as painful circumscribe
d ulcer with a ragged edge; Hence the term geni
tal ulcer disease
• Most of the ulcers are on the external genitalia
• Diagnosis: By isolation of H. ducreyi from the ulc
ers
• Treatment: Tcl, Augmentin, Cotrimoxazole, Eryth
romycin, Ceftriaxone
Part IV:
Spirochaetes
• Family: Spirochaetaceae. Is composed of
5 genera>>Treponema, Spirochaeta, Borr
elia, Leptospira & Cristispira
• 3 genera of medical importance:Borrelia, T
reponema, Leptospira
(turning thread),  (thin spiral)
Morphology
• spiral shaped organisms, lack flagella,
but are motile by means of rotatory & bend
ing movements. Only Leptospira is cultiva
ble in lab media
T. pallidum
• Genus: Treponema. Species:T. pallidum
• Morphology:Treponema pallidum is a Gram-
negative bacteria which is spiral in shape. It is
an obligate internal parasite, pathogenic Trep
onemes have tapered ends oriented toward
host cell surface during attachment, 5-20µm l
ength & 0.09-0.5µm in diameter with 8-14 eve
nly distributed waves per each cell. Produce
hyalluronidase, glycolipids & oxidase
Growth
• Do not grow in artificial culture, but can be
propagated in the testes of rabbit or chim
panzee in reduced o2 tension
• Do not stain by Grams method but will tak
e up Silver nitrate stains, & can also be de
monstrated by dark-ground microscopy
• Sensitive to heat, die at 41°C & above
Antigenic structure
• Little is known because organisms can not be cu
ltured in lab media
• Cardiolipin which is thought to be antigenic com
ponent is also present in mammalian heart musc
le
• It is not known whether cardiolipin the antigen th
at stimulates production of Wassermann antibod
y in VDRL test or is released from mammalian ti
ssues during active treponemal infection
Syphilis
• T. pallidum causes syphilis, a sexually tran
smitted disease but transmission can also
occur between mother and child in utero; t
his is called congenital syphilis
• Syphilis was discovered in 1905 by Schau
dinn & Hoffman
• In 1906 Wassermann introduced the diag
nostic serologic test that bears his name to
date
Pathogenesis
• Acquired by sexual contact
• Accidental infection can occur by contact
with infectious lesions /materials
• Congenital infections can arise from trans-
placental spread of spirochaetes during th
e last trimester of pregnancy
Clinical manifestations
• a) Primary syphilis
– Incubation: 10-90 days
– First sign is chancre (hard indurated papule)
– It soon ulcerates>> painless lesion
– In 4-10 weeks the lesion heals
– Most chancre are on external genitalia
– Sometimes appear on other parts of the body
Primary chancre
Primary Chancre
Primary Chancre
Clinical manifestations cont.
• b) Secondary syphilis
– Lesions of skin & mucosae 6-8 weeks after th
e chancre
– At this stage lesion swarm with spirochaetes,
& are highly infectious
• c) Tertiary syphilis
– Signs develop between 3-20 years or more aft
er initial infection
– Lesions: gummata, cardiovascular lesions &
meningovascular lesions
Secondary syphilis rash on the back.

Secondary syphilis
Secondary Syphilis
Clinical manifestations cont.
• CNS lesions, such as tabes dorsalis & gen
eral paralysis of the insane (GPI) >> know
n as Neuro-syphilis
• Late neurosyphilis>> paralytic dementia, s
eizures, optic atrophy
• Late cardiovascular syphilis>> angina pect
oris, myocardial insufficiency & >> death
Congenital Syphilis
• Trans-placental infection of the developing
fetus
• Takes place from the 19th week of gestatio
n>> transmission does not take place until
the 5th month of gestation
• Transmission is more in primary than seco
ndary syphilis
Symptoms of Congenital Syphili
s
• Jaundice, hemolytic anaemia
• hepatosplenomegaly
• pneumonia
• multiple long bone involvement
• skin lesions
• snuffles & testicular masses are common
sometimes with severe dehydration & mal
nutrition
Manifestations of congenital syp
hilis
• High palatal arch, saddle nose, short maxil
la, protuberance of mandible, frontal bossa
e of parrot and Hutchinson’s triad
Diagnosis
• 1) Dark ground microscopy
• 2) Reagin serological tests: Depend on a s
erological cross reaction between antibodi
es to T. pallidum & an antigen called “cardi
olipin” prepared from normal ox heart mus
cle’ thus there is:
– Wassermann reaction>> compliment fixation r
eaction. Used formally, now has been supers
eded by simpler flocculation reactions
Diagnosis cont.
– VDRL (Venereal Disease Research Laborator
y) test>> is a flocculation reaction. It is now a
standard reagin type test for syphilis
Biological false positive VDRL
• Viral infections:
– Measles, varicella(chicken pox), hepatitis
• Protozoal infections:
– Malaria, trypanosomiasis
• Bacterial infections: Tb, leprosy
• Chlamidial & Rickettsial infections
• Non-syphilitic spirochaetal infections:
– Yaws, bejel, pinta, leptospirosis
• Non-infectious conditions: pregnancy, rheumatoi
d arthritis
Specific serological tests
• i) Treponema pallidum immobilization test(
TPI)
• ii) Treponema pallidum haemoglutination t
est (TPHA)
• iii) Fluorescent treponemal antibody test
Note: In all of the above tests ‘treponemal
antigen’ is used instead of cardiolipin
Treatment
• Benzyl penicillin is a drug of choice
• Every effort should be made to rule out penicillin
allergy before choosing other antibiotics
• Other drugs: Tcl, Erythromycin and cephalospori
ns (cephaloridin & cephalothin
• Primary syphilis treatment of penicillin 10-14 day
s, late syphilis at least 21 days. Longer therapy
with Tcl may cause damage to the long bones &
teeth
Jarisch-Herxheimer Reaction
• Happens 2-12 hours following the treatme
nt of active (primary) syphilis
• Some people develop an acute focal & sys
temic reaction characterised by headache,
malaise & fever
• In late syphilis the reaction is insignificant
Part V:
Trichomoniasis
• Aetiology: Trichomonas vaginalis is a protozoa
• Incubation period: 4/7 – 3/52 following sexual int
ercourse
• Clinical features: severe pruritis and purulent va
ginal or urethral discharges
• Diagnosis: examination of the dicharge microsco
pically for T. vaginalis
• Treatment:Metronidazole(Flagyl) Tinidazole
Part VI:
HIV / AIDS
• What is HIV?
• What is AIDS?
• How does HIV replicate? Pathogenesis of HIV
• How is HIV transmitted?
• Clinical features and stages of HIV
• Which tests are used to diagnose HIV infection?
• How is the HIV positive patient treated?
HIV / AIDS
• HIV control/ prevention
• Opportunistic infections in HIV positive pati
ents
• Impact of HIV/ AIDS
HIV
• HIV:
– Human Immunodeficiency Virus. This is the vi
rus which causes AIDS. It is a retrovirus, mea
ning that its genetic information is stored on si
ngle-stranded RNA instead of the double-stra
nded DNA found in most organisms
AIDS
• AIDS:
– Acquired Immuno Deficiency Syndrome. It is a
collection of diseases that are seen in a patie
nt as a result of the virus weakening the body
immune system
Stages of HIV reproduction
– HIV binds to receptors & enters the CD4+ cell
– HIV uses an enzyme known as “reverse trans
criptase” to convert its RNA into DNA
– HIV enters the nucleus of the CD4+ cell & ins
erts itself into the cell’s DNA
– HIV DNA then instructs the cell to make many
copies of the original virus
Stages of HIV reproduction Cont…

• With the help of the “protease” enzyme ne


w virus particles are assembled
• CD4+ cell burst
• Assembled viruses leave the cell, ready to
infect other CD4+ cells
The Structure of HIV
• Outside of a human cell, HIV exists as rou
ghly spherical particles (sometimes called
virions). The surface of each particle is stu
dded with lots of little spikes.
The Structure of HIV Cont…
• An HIV particle is around 100-150 billionth
s of a metre in diameter. That's about the s
ame as:
• 0.1 microns
• 4 millionths of an inch
• one twentieth of the length of an E. coli ba
cterium
• one seventieth of the diameter of a human
CD4+ white blood cell.
The Structure of HIV Cont…
• HIV belongs to a special class of viruses called r
etroviruses. Within this class, HIV is placed in th
e subgroup of lentiviruses. Other lentiviruses incl
ude SIV, FIV, Visna and CAEV, which cause dis
eases in monkeys, cats, sheep and goats. Almo
st all organisms, including most viruses, store th
eir genetic material on long strands of DNA. Retr
oviruses are the exception because their genes
are composed of RNA (Ribonucleic Acid)
The Structure of HIV Cont…
• RNA has a very similar structure to DNA.
However, small differences between the t
wo molecules mean that HIV's replication
process is a bit more complicated than tha
t of most other viruses
How many genes does HIV have
?
• HIV has just nine genes (compared to more than
500 genes in a bacterium, and around 20,000-2
5,000 in a human). Three of the HIV genes, calle
d gag, pol and env, contain information needed t
o make structural proteins for new virus particles
. The other six genes, known as tat, rev, nef, vif,
vpr and vpu, code for proteins that control the ab
ility of HIV to infect a cell, produce new copies of
virus, or cause disease
Structure cont…
• At either end of each strand of RNA is a se
quence called the long terminal repeat, wh
ich helps to control HIV replication.
Transmission of HIV

– Sexual transmission
– Transfusion of infected blood & blood product
s
– Maternal transmission, during delivery & brea
st feeding
– Transmission through HIV-contaminated instr
uments e.g. needles, acupuncture & tattoos
– Mucocutaneous/ cutaneous exposure
Clinical features & Stages of HIV

– Major signs and symptoms:


• Fever for more than one month
• Weight loss more than ten percent

– Minor signs and symptoms:


• Cough for one month without evidence of TB
• Generalized pruritic dermatitis
• Oral-pharyngeal candidiasis
• Generalized lymphadenopathy
Minor signs and symptoms Cont…

• Kaposi’s sarcoma
• Mental confusion
• Herpes zoster and
• Herpes simplex
HIV Stages Cont…
• Clinically HIV is grouped into 4 stages acc
ording to severity (WHO):
– Asymptomatic stage
– Mild disease stage
– Moderate disease stage
– Severe disease stage
Commonly used tests to diagnose
HIV
• ELISA: This is the initial screening test. It tests p
resence of antibodies against HIV. Positive resul
ts obtained within 3 months of acquiring infection
• Western Blot: This is a confirmatory test. It dete
cts antibodies against antigens coded by 3 differ
ent viral genes
• Determine HIV-1/2 : This is an immuno-chromat
ographic test for the qualitative detection of antib
odies to HIV-1 and HIV-2
• Polymerase chain reaction (PCR) assays:
• Used to assay for both HIV RNA and HIV DNA
Treatment of HIV/AIDS
• Two major classes of antiretroviral drugs:
– Reverse transcriptase inhibitors (RTIs):
• Nucleoside Reverse Transcriptase Inhibitors
• Non- Nucleoside Reverse Transcriptase Inhibitors
– Protease inhibitors (PIs)
• Management of opportunistic infections in
AIDS
Nucleoside Reverse Transcriptase
Inhibitors (NRTIs)
– Zidovudine (AZT, retrovir)
– Didanosine (DDI, videx)
– Lamivudine (3TC, epivir)
– Stavudine (D4T, zerit, stavir)
– Abacavir (ABC, ziagen)
– Zalcitabine (DdC, hivid)
Non Nucleoside Reverse Transcript
ase Inhibitors (NNRTIs)
– Efavirenz (EFV, sustiva, stocklin)
– Delaviridine (DLV, rescriptor)
– Nevirapine (NVP, viramune)
Protease Inhibitors (PIs)
– Saquinavir- HGC (Invirase)
– Saquinavir- SGC (Fortovase)
– Ritonavir (Norvir)
– Indinavir (Crixivan)
– Nelfinavir (Viracept)
– Amprenavir (APV agenerase)
Combination Therapies
– 2NRTIs + 1 NNRTI(once daily kit):
• Odivir kit (Efavirenz 600mg + Lamivudine 300mg +
Didanosine 250/ 400mg)
– 2NRTIs + 1 NNRTI (Fixed dose combination):
• Triomune (Lamivudine150mg + Nevirapine 200mg
+ Stavudine 30/ 40mg)
• Duovir-N (Lamivudine 150mg + Zidovudine 300mg
+ Nevirapine 200mg)
Combination Therapies Cont…
• 2PIs:
– Kaletra (Lopinavir + Ritonavir)
• 2NRTIs:
– Lamivir-S (Lamivudine 150mg + Stavudine 30
/40mg)
– Duovir or Combivir (Lamivudine 150mg + Zido
vudine 300mg)
Undesired Drug Reactions
– SE: Rashes
– ADR: Steven Johnson Syndrome
– Drug Interactions: Not to be taken together wit
h Rifampicin, PI, and birth control pills
Drug Resistance
• Drug quality, patients missing doses, and i
mproper use of antiretroviral drugs or usin
g drugs too early in the course of the disea
se, can all lead to drug resistance
Opportunistic infections in HIV
• Bacterial infections:
– TB, diarrhoea, Typhoid fever
• Fungal:
– Cryptococcal meningitis, Candidiasis(oral and
vaginal)
• Parasitic:
• Pneumocysti carni pneumonia* (PCP)
, & Malaria
Viral: Herpes zoster or herpes simplex
Opportunistic Infections cont.
• Cancer:
– Kaposi’s sarcoma (a known skin cancer)
– Lymphomas- Brain lymphoma
Part VII:
Venereal Warts
• Causative agents: Papiloma virus (Verruca vulga
ris)
• This is a DNA virus, 40-60nm in diameter, with a
n icosahedral capsid composed of 72 capsomer
s
• Attempts to culture them in vitro have been unsu
ccessful
• The spread is faster in non-immune persons
• Treatment: In severe cases the warts may be re
moved by chemical or physical means e.g. burni
ng with Silver nitrate sticks or Podophylline, or b
y rays
The End

• Thank you for your atte


ntion

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